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本研究探讨汉防己甲素(Tet)、雌激素受体抑制剂托瑞米芬(Tor)及其联合应用对K562/A02细胞多药耐药的逆转作用。采用噻唑蓝法(MTT)测定阿霉素(ADR)的半数抑制量,RT-PCR法检测MDR1基因mRNA表达水平,FCM检测P-gp的表达和细胞内ADR浓度。结果表明:ADR对K562/A02和K562细胞的IC50分别为57.43和1.16mg/L,Tet(1μmol/L)和Tor(2.5μmol/L)单用及两药联用处理K562/A02细胞时,ADR的IC50值分别为14.12,20.74和9.14mg/L。Tet及Tor单独作用后耐药株MDR1 mRNA下调微弱,联合用药下调效果明显。Tet及Tor均可降低P-gp蛋白的表达,且具有协同作用。Tet及Tor作用后细胞内ADR浓度增加,两药联合作用时效果增强。结论:Tet及Tor均可逆转K562/A02细胞多药耐药,联合作用时效果增强。
This study was designed to investigate the reversal of multidrug resistance in K562 / A02 cells by combining tetrandrine (Tet) and estrogen receptor inhibitor torremifene (Tor) and their combination. The half inhibition of adriamycin (ADR) was determined by MTT assay. The mRNA expression of MDR1 was detected by RT-PCR. The expression of P-gp and the concentration of intracellular ADR were detected by FCM. The results showed that IC50 of ADR was 57.43 and 1.16mg / L for K562 / A02 and K562 cells, respectively. When K562 / A02 cells were treated with Tet (1μmol / L) and Tor (2.5μmol / The IC50 values for ADR were 14.12, 20.74 and 9.14 mg / L, respectively. After Tet and Tor alone, the down-regulation of MDR1 mRNA in drug-resistant strain was weak and the combination therapy significantly reduced the effect. Both Tet and Tor can reduce the expression of P-gp protein and have a synergistic effect. After the action of Tet and Tor, the intracellular ADR concentration increased, and the combination of the two drugs enhanced the effect. CONCLUSION: Both Tet and Tor can reverse the multidrug resistance of K562 / A02 cells, and the effect is enhanced when combined with Tet.